We highlight that infertility in Cdk5rap2 mutant mice is secondary to a lack of spermatogenic cells in adult mice as a result of an early developmental defect in the germ cells through mitotic delay, prolonged cell cycle, and apoptosis.

mouse expresses only one form of CDK5RAP2 that is equivalent to the human and rat alternatively spliced variant forms

this study revealed the presence of previously unknown splice variants of the Cdk5rap2 gene that are at least in part accountable for the lack of microcephaly in the mice.

In Cdk5rap2-depleted neural embryonic stem cells there is an increase in cell death in differentiating cells.

Mouse expression pattern of CDK5RAP2 is similar to that seen in humans and is in concordance with pathology suggested by neuroimaging studies in humans and mouse

This study demonistrated that CDK5RAP2 is a key molecule that mediates functional interaction and is essential for centrosomal targeting of Aurora-A (zeige AURKA ELISA Kits).

Cdk5rap2 is highly expressed in the neural progenitor pool and its loss results in a depletion of apical progenitors and increased cell-cycle exit leading to premature neuronal differentiation

The an mutation is a genomic inversion of exon 4 of Cdk5rap2, resulting in an in-frame deletion of exon 4 from the mRNA. Cdk5rap2(an/an) neuronal precursors exit the cell cycle prematurely and many undergo apoptosis.

CDK5RAP2 Antigen-Profil

Beschreibung des Gens

This gene encodes a regulator of CDK5 (cyclin-dependent kinase 5) activity. The protein encoded by this gene is localized to the centrosome and Golgi complex, interacts with CDK5R1 and pericentrin (PCNT), plays a role in centriole engagement and microtubule nucleation, and has been linked to primary microcephaly and Alzheimer's disease. Alternative splicing results in multiple transcript variants.